Cardiogenic shock following cardioversion of atrial flutter

Introduction with a case

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Once upon a time at Genius General Hospital a 63-year-old woman was admitted with lower extremity edema and orthopnea. Her past medical history was unremarkable. She was noted to be in atrial flutter with a heart rate in the 120s and a blood pressure ranging from 100-120 mm systolic. She was admitted to the medicine ward. Transthoracic echocardiogram revealed an ejection fraction of 18% with diffuse hypokinesis.

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Attempts were made to control her heart rate with diltiazem and later metoprolol, but these were unable to control her heart rate without causing hypotension. After several days on the medicine ward, she was taken for trans-esophageal echocardiogram followed by cardioversion.

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Prior to cardioversion she was receiving metoprolol 7.5 mg IV every six hours and furosemide. Her vital signs prior to procedure were Bp 115/70 and heart rate 130 b/m. Following a single 100 Joule shock she was successfully cardioverted into normal sinus rhythm at a rate of 65 b/m. Immediately after cardioversion her blood pressure fell to the 60s-70s systolic requiring initiation of a phenylephrine infusion and transfer to the ICU. The only medication used for procedural sedation was propofol. In the ICU she was noted to be in cardiogenic shock with poor urine output, and was transitioned to dobutamine. After two days she was able to be weaned off dobutamine, at which time her blood pressure was 100/70 with a heart rate of 80 b/m in normal sinus rhythm.

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She remained in sinus rhythm and continued to gradually improve. Repeat imaging several weeks later revealed that her ejection fraction increased to 42%. Ischemic evaluation was negative.

Following cardioversion, her heart rate decreased by a factor of two, from 130 b/m to 65 b/m. Although her stroke volume may have improved a bit, it certainly did not double. Her stroke volume was limited more by systolic dysfunction than by poor diastolic filling, so it was unlikely to benefit dramatically from cardioversion. Given that her heart rate decreased by a factor of two without any major improvement in her stroke volume, her cardiac output and blood pressure decreased substantially.

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Predicting the hemodynamic effect of cardioversion

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Cardioversion may cause cardiac output and blood pressure to improve or deteriorate. When faced with a critically ill patient with supraventricular tachycardia, it is important to consider how likely cardioversion is to improve hemodynamics.

Cardioversion usually decreases heart rate. In order to cause a hemodynamic improvement, the stroke volume must improve sufficiently to out-weight the reduction in heart rate. The heart rate above which diastolic filling and stroke volume deteriorate is unclear and likely varies between patients. ACLS guidelines suggest that when the heart rate is <150 b/m it is unlikely that hemodynamic instability is due primarily to the tachycardia unless there is impaired ventricular function. Heart rate may be the single most important predictor of how cardioversion will affect hemodynamics. The higher the heart rate is, the more likely diastolic filling is compromised and will improve following cardioversion.

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Other factors also matter. A patient with new-onset atrial fibrillation (AF) may regain atrial contraction, whereas a patient who has been in AF for some time may develop atrial tachymyopathy and require weeks to regain atrial contraction. Patients with pulmonary hypertension, mitral stenosis, or diastolic dysfunction may benefit more from restoration of sinus rhythm.

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Overall, cardioversion is generally well tolerated and often improves hemodynamics. However, there are occasional patients with severe cardiac dysfunction who need a compensatory tachycardia, and may decompensate if pushed into a slow sinus rhythm. There is little recent evidence on hemodynamic changes after cardioversion. Upshaw 1997reviewed literature on hemodynamic changes after cardioversion of AF lasting at least 10 days, and found that cardiac output often decreased with 1.2% of patients developing acute pulmonary edema.

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Patients in atrial flutter are less likely to improve hemodynamically following cardioversion, as their rate is usually not much higher than 150 b/m. Additionally, flutter is generally a regular rhythm which causes less impairment of ventricular function.

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Target heart rate for atrial fibrillation patient in septic shock?

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Similar considerations apply to a patient with chronic AF in septic shock. Lowering the heart rate to a “normal” range (i.e., 60-100 b/m) will worsen cardiac output. It may be sensible to allow patients in septic shock to have a permissive tachycardia in the 110s-130s range. Among outpatients, the RACE-II trial demonstrated that lenient rate control (targeting a resting heart rate <110 b/m) was non-inferior to a strict rate-control strategy (targeting a resting heart rate <80 b/m), suggesting that mild tachycardia may be well tolerated (Van Gelder 2010).

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Final thoughts on the case

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In retrospect it’s not surprising that this woman with an ejection fraction of 18%, marginal blood pressure, beta-blockade, and atrial flutter at a rate of 130 b/m might develop shock following cardioversion. Patients with severe systolic dysfunction require cautious management as they may be destabilized by interventions which are otherwise well tolerated (i.e., beta-blockers). Her creatinine was rising prior to cardioversion, suggesting that her systemic perfusion was already tenuous.

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However, she likely had a component of tachycardia-induced cardiomyopathy and did ultimately benefit from cardioversion with marked improvement in her ejection fraction. Atrial flutter may be harder to rate-control than atrial fibrillation, given the fixed nature of the atrial re-entrant circuit. Rate vs. rhythm control in heart failure is controversial, but given the difficulties controlling her heart rate a trial of sinus rhythm was reasonable. Discontinuing the metoprolol prior to cardioversion may have reduced the extent of post-cardioversion hypotension, by allowing her heart to develop a compensatory tachycardia after cardioversion and avoiding negative inotropic effects.

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Take-home messages

Hemodynamic improvement after cardioversion is more likely when the initial heart rate is very fast. Patients with a heart rate under 150 b/m are less likely to improve immediately following cardioversion.

Patients treated with negative chronotrophic agents prior to cardioversion may be pushed in a slow sinus rhythm without the ability to mount a compensatory sinus tachycardia.For patients with severe systolic dysfunction, this can precipitate cardiogenic shock.

For patients with chronic AF in septic shock, attempting to “normalize” the heart rate will reduce the cardiac output. Such patients may benefit from permissive tachycardia.

(PS: Don’t interpret this post to mean that I don’t like cardioversion. I love cardioversion. Will have more to say about this in future posts – stay tuned.)

– doctors are obsessed with fixing figures instead of developping a pathophysiology thinking. Same problem with postoperative AF : too much automatic medications instead of understanding the situation my post here : http://www.nfkb0.com/2014/02/19/fibrillation-auriculaire-en-post-operatoire/ i guess a web translator may help non french reader 😉 )– why in the hell did they use diltiazem and metoprolol with such a poor EF ?– i only know one indication of phenylephrine :hypotension during a c section with a perimedullar anesthesia– thank you so much fort saying that slowing down a patient in septic shock (and AF) is really a bad idea, especially at the acute phase. The "new" litterature on this subject tempts the youngest docotrs and this frightens me

I agree with your suprise about using metoprolol or diltiazem with such a low ejection fraction. Technically beta-blockers are indicated for AF with heart failure. Of course, if the heart failure is very severe, the patient will be unable to tolerate beta-blockade. It can be tricky sorting out which patients will be able to tolerate beta-blockade. Perhaps a short-acting agent like esmolol may be useful in situations where there is doubt, as it may be discontinued rapidly if not tolerated.

I agree that the indications for phenylephrine are quite limited. I will occasionally use it for AF with rapid ventricular response and severe hypotension (to avoid aggrevating the tachycardia with excess beta-stimulation). Overall, phenylephrine is probably overused and it carries a risk of making the blood pressure look better without actually improving cardiac output (thereby fixing the numbers but not really improving the patient).

Great Post! In my opinion, the decision to cardiovert should be Echo-guided. As you say quite well:

“In order to cause a hemodynamic improvement, the stroke volume must improve sufficiently to out-weight the reduction in heart rate. The heart rate above which diastolic filling and stroke volume deteriorate is unclear and likely varies between patients.”

I find that the Echo elucidates this question. If the echo shows a great EF, yet poor Stroke Volume due to significantly decreased LV filling (that appears to be a result of the tachycardia), these patients are likely to benefit from cardioversion. Conversely, if the echo reveals decent LV filling, yet poor EF, these patients are unlikely to benefit from cardioversion. I often find that comparing the “before and after” cardioversion Echo to be quite telling in this regard!